Evidence map›Paper›PMID 9751747›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

LCK-phosphorylated human killer cell-inhibitory receptors recruit and activate phosphatidylinositol 3-kinase.

F Marti, C W Xu, A Selvakumar, R Brent, B Dupont, P D King

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. CD8αα homodimers function as a coreceptor for KIR3DL1.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Review
  7. Review
  8. Functional NK cell repertoires are maintained through IL-2Rα and Fas ligand.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. ITAMs versus ITIMs: striking a balance during cell regulation.The Journal of clinical investigation · 2002
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

F MartiThe Immunology Program, Memorial Sloan-Kettering Cancer Center, Cornell University Medical Center, New York, NY 10021, USA.
C W Xu
A Selvakumar
R Brent
B Dupont
P D King
Massachusetts General Hospital · USHospital for Special Surgery · USHarvard University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Elisa de Stanchina · 1985 to 2026
$347.4M
CD28 MEDIATED ACTIVATION SIGNALSR01AI037294 · NIAID · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DUPONT, BO · 1995 to 1997
–
NCI NIH HHS CA08748NCI NIH HHS P30 CA008748NIAID NIH HHS AI37294
6 · The paper itself

Abstract

HLA-specific killer cell inhibitory receptors (KIR) are thought to impede natural killer (NK) and T cell activation programs through recruitment of the SH2 domain-containing tyrosine phosphatases, SHP-1 and SHP-2, to their cytoplasmic tails (CYT). To identify other SH2 domain-containing proteins that bind KIR CYT, we used the recently described yeast two-bait interaction trap and a modified version of this system, both of which permit tyrosine phosphorylation of bait proteins. Using these systems, we show that KIR CYT, once phosphorylated by the src-family tyrosine kinase LCK, additionally bind the p85alpha regulatory subunit of phosphatidylinositol (PI) 3-kinase. Furthermore, we show that in an NK cell line, NK3.3, cross-linking of KIR results in recruitment of p85alpha to KIR and activation of PI 3-kinase lipid kinase activity. One consequence of KIR coupling to PI 3-kinase is downstream activation of the antiapoptotic protein kinase AKT. Therefore, in addition to providing negative signals, KIR may also contribute positive signals for NK and T cell growth and/or survival.

Indexed as

Protein Serine-Threonine KinasesCell LineEnzyme ActivationHumansIntracellular Signaling Peptides and ProteinsKiller Cells, NaturalLymphocyte Specific Protein Tyrosine Kinase p56(lck)Phosphatidylinositol 3-KinasesPhosphorylationProtein ConformationProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, ImmunologicAKT1 protein, humanIntracellular Signaling Peptides and ProteinsLymphocyte Specific Protein Tyrosine Kinase p56(lck)Phosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTPN11 protein, humanPTPN6 protein, humanReceptors, ImmunologicReceptors, KIRSH2 Domain-Containing Protein Tyrosine Phosphatases

Identifiers

PMID9751747
PMCPMC21722
OpenAlexW1993019351

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.